1. Technical Field
The present invention relates to apparatus and methods for non-invasively determining oxygen saturation in blood in general, and to apparatus and methods for non-invasively determining oxygen saturation in venous blood in particular.
2. Background Information
Arterial blood oxygen saturation (SaO2) can be determined by pulse oximetry or co-oximetry measurements of arterial blood. Pulse oximetry, for example, is a well established non-invasive technique for determining a SaO2 value. Most subjects have a SaO2 value in the range of 95-100%. Central venous blood oxygen saturation (ScvO2) and mixed venous blood oxygen saturation (SmvO2), both types of composite venous blood oxygen saturation (SvO2), are measurements of the relationship between oxygen consumption and oxygen delivery in the body. Normal values of mixed venous oxygen saturation (SmvO2) are 60-80% O2 saturation. Central venous oxygen saturation (ScvO2) values represent regional venous saturations with a normal value of about 70% and historically have been measured invasively just outside the heart, usually in the superior vena cava (SVC). ScvO2 usually measures slightly higher than SmvO2 as it has not mixed with the venous blood from the coronary sinus draining into the right atrium. Although the values may differ, they trend together.
Mixed venous oxygen saturation (SmvO2) is far more difficult to determine than arterial blood oxygen saturation (SaO2). Pulmonary artery saturation is an accurate indicator of SmvO2. The pulmonary artery blood includes venous blood returning to the heart via the superior vena cava (SVC) and via the inferior vena cava (IVC). From there, blood enters the right atrium and into the right ventricle where it is mixed. Since the SVC and IVC oxygen saturations can be different, the resultant oxygen saturation in the right ventricle and into the pulmonary artery is a mixed value likely between SVC and IVC oxygen saturations. However, obtaining a pulmonary artery blood oxygen saturation value or right ventricle oxygen saturation value is difficult and must be done invasively; e.g., requires a catheter be placed to access these sites.
Accurately determining the adequacy of tissue oxygenation in critically ill patients can be vital to patient treatment. Tissue hypoxia or imbalances between whole-body oxygen supply and demand can occur even when the subject has normal blood pressure, central venous pressure, heart rate, and blood gas values. It is desirable, therefore, to have more direct indicators of tissue oxygen saturation; e.g., mixed and central venous oxygen saturations.
A normal cardiovascular response of increasing oxygen consumption (VO2) is to increase O2 extraction from the blood and/or increase cardiac output (CO). Oxygen consumption is typically independent of oxygen delivery (DO2), since tissues can satisfy oxygen requirements by increasing O2 extraction when DO2 decreases. However, once a critical DO2 compensatory increase in O2 extraction is reached, the ability to satisfy oxygen consumption is dependent on DO2. If oxygen consumption requirements cannot be met, then tissue hypoxia can Occur.
A decrease in SmvO2 and ScvO2 can represent an increased metabolic stress. For example, metabolic stress can occur if DO2 does not increase in such a way to cover an increased VO2, or if DO2 drops because of decrease in either arterial O2 content, cardiac output, or both. The magnitude of the decrease indicates the extent to which the physiological reserves are stressed:
SmvO2 > 75%Normal Extraction: O2 supply > O2 demand75% > SmvO2 > 50%Compensatory Extraction: Increase in O2demand, or decrease in O2 supply50% > SmvO2 > 30%Exhaustion of Extraction; beginning of lacticacidosis; O2 supply < O2 demand30% > SmvO2 > 25%Severe lactic acidosisSmvO2 < 25%Cellular deathThe cardiocirculatory system may be challenged by a drop in DO2 that is induced by anemia, hypoxia, hypovolemia, or heart failure. Fever, pain, or stress can also decrease SmvO2 or ScvO2 by increasing whole-body VO2.
Historically, mixed venous oxygen saturation (SmvO2) values have been invasively obtained using a pulmonary artery catheter, and central venous oxygen saturation (ScvO2) values have been invasively obtained using a central venous catheter. The ScvO2 value reflects the degree of oxygen extraction from the brain and the upper part of the body. The SmvO2 value reflects the relationship between whole-body O2 consumption and cardiac output.
A central venous blood sampling (e.g., from the superior vena cava) reflects the venous blood of the upper body but neglects venous blood from the lower body (i.e., intra-abdominal organs). Venous O2 saturation values can differ among several organ systems since the organs extract different amounts of O2. ScvO2 is usually less than SmvO2 by about 2-3% because the lower body extracts less O2 than the upper body, making inferior vena cava O2 saturation higher. The primary cause of the lower O2 extraction is that many of the vascular circuits that drain into the inferior vena cava use blood flow for nonoxidative phosphorylation needs (e.g., renal blood flow, portal flow, hepatic blood flow, etc.). However, SmvO2 and ScvO2 change similarly when the whole body ratio of O2 supply to demand is altered.
The difference between the absolute value of ScvO2 and SmvO2 can change, however, when the patient is in shock. In septic shock, ScvO2 often exceeds SmvO2 by about 8%. During cardiogenic or hypovolemic shock, mesenteric and renal blood flow decreases and an increase in O2 extraction in these organs typically follows. During septic shock, regional O2 consumption of the gastrointestinal tract (and therefore regional O2 extraction) increases despite elevated regional blood flows. On the other hand, cerebral blood flow is maintained over some period in shock. This characteristic can cause a delayed drop of ScvO2 in comparison to SmvO2, and the correlation between these two parameters could worsen as a result. It should be noted, however, that venous oximetry can provide accurate information on the adequacy of tissue oxygenation only if the tissue is still capable of extracting O2. In the case of arteriovenous shunting on the microcirculatory level or cell death, SmvO2 and ScvO2 may not decrease or may even show elevated values despite severe tissue hypoxia; e.g., patients with prolonged cardiac arrest have experienced venous hyperoxia, despite test results showing a ScvO2 higher than 80% which is indicative of impaired oxygen use.
The ability to determine a composite venous oxygen saturation value (SvO2) can facilitate the determination of other information, such as the cardiac output of a subject. The Fick Principle provides that blood flow to an organ can be calculated using a marker substance if the following information is known: a) the amount of marker substance taken up by the organ per unit time; b) the concentration of the marker substance in the arterial blood supplying the organ; and c) the concentration of the marker substance in venous blood leaving the organ. Using Fick's original method, the cardiac output (“CO”) of a subject could be measured by determining the oxygen consumption (“VO2”), the oxygen content of the blood taken from the pulmonary artery (“Cv”; i.e., mixed venous blood), and the oxygen content of the blood from a peripheral artery (“Ca”; i.e., arterial blood). The VO2 could be determined using a spirometer within a closed rebreathing circuit incorporating a CO2 absorber. The Ca and Cv values could be determined by evaluating blood samples invasively taken from the subject. From these values, the VO2 can be expressed as:VO2=(CO×Ca)−(CO×Cv)  (Eqn. 1)The above relationship can be manipulated as follows:
                    CO        =                              VO            2                                              C              a                        -                          C              v                                                          (                  Eqn          .                                          ⁢          2                )            and the cardiac output calculated. In reality, however, this method is impractical and rarely used due to the difficulty of collecting and analyzing the O2 concentrations within the sample.
What is needed is an apparatus and method that can be used to determine the oxygen saturation of venous blood (SvO2) at any location within a subject's body, and one that can be specifically used to non-invasively determine a mixed venous oxygen saturation value (SmvO2) and a central venous oxygen saturation (ScvO2) value.